Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2006-6-5
pubmed:abstractText
Acute and chronic alcohol abuse impairs various functions of the immune system and thus, has been implicated as a cofactor in the immunopathogenesis of human immunodeficiency virus (HIV) disease progression. We determined whether naltrexone, an opioid receptor antagonist widely used in the treatment of alcoholism, inhibits alcohol-mediated enhancement of HIV infection of T cells. Alcohol enhanced HIV infection of peripheral blood lymphocytes (PBL) and a human lymphoid cell line (CEMX174). Alcohol increased HIV X4 envelope (Env), not murine leukemia virus Env-pseudotyped infection of CEMX174 cells. Naltrexone antagonized the enhancing effect of alcohol on HIV infection of PBL and CEMX174 cells. The specific mu-opioid receptor antagonist, Cys2, Tyr3, Arg5, Pen7 (CTAP) amide, also blocked the enhancing effect of alcohol on HIV infection. Investigation of the underlying mechanism for the alcohol action showed that alcohol significantly increased endogenous beta-endorphin production and induced mu-opioid receptor mRNA expression in PBL and CEMX174 cells. The role of beta-endorphin in alcohol-mediated enhancement of HIV infection was indicated by the observations that naltrexone and CTAP antagonized ether alcohol- or exogenous beta-endorphin-mediated enhancement of HIV infection. These findings suggest a biological mechanism for the potential therapeutic benefit of naltrexone in treating HIV-infected alcoholics.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0741-5400
pubmed:author
pubmed:issnType
Print
pubmed:volume
79
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1166-72
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:16574767-Adult, pubmed-meshheading:16574767-Alcohol Deterrents, pubmed-meshheading:16574767-Alcoholism, pubmed-meshheading:16574767-Cells, Cultured, pubmed-meshheading:16574767-Disease Susceptibility, pubmed-meshheading:16574767-Drug Evaluation, Preclinical, pubmed-meshheading:16574767-Ethanol, pubmed-meshheading:16574767-Female, pubmed-meshheading:16574767-HIV Infections, pubmed-meshheading:16574767-HIV Reverse Transcriptase, pubmed-meshheading:16574767-HIV-1, pubmed-meshheading:16574767-Humans, pubmed-meshheading:16574767-Hybrid Cells, pubmed-meshheading:16574767-Leukemia Virus, Murine, pubmed-meshheading:16574767-Lymphocytes, pubmed-meshheading:16574767-Male, pubmed-meshheading:16574767-Middle Aged, pubmed-meshheading:16574767-Naltrexone, pubmed-meshheading:16574767-Peptide Fragments, pubmed-meshheading:16574767-Peptides, pubmed-meshheading:16574767-RNA, Messenger, pubmed-meshheading:16574767-Receptors, Opioid, mu, pubmed-meshheading:16574767-Somatostatin, pubmed-meshheading:16574767-T-Lymphocytes, pubmed-meshheading:16574767-Up-Regulation, pubmed-meshheading:16574767-Virion, pubmed-meshheading:16574767-Virus Replication, pubmed-meshheading:16574767-beta-Endorphin
pubmed:year
2006
pubmed:articleTitle
Naltrexone inhibits alcohol-mediated enhancement of HIV infection of T lymphocytes.
pubmed:affiliation
Division of Allergy and Immunology, Joseph Stokes Jr. Research Institute at the Children's Hospital of Philadelphia, 34th Street & Civic Center Boulevard, Philadelphia, PA 19104, USA.
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural